ArticleScience signaling2023
Enteric glia promote visceral hypersensitivity during inflammation through intercellular signaling with gut nociceptors.
Article in Science signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- TREM-1-dependent macrophage infiltration mediates visceral hypersensitivity via vlPAG GABAergic neuron activation in a mouse model of inflammatory bowel disease.Cellular & molecular biology letters · 2026Article
- Connexin-43-Mediated Gap Junction Coupling Between Adipocytes Regulates Norepinephrine-Induced CaCells · 2026Article
- Neuro-immune interactions in gastrointestinal oncology: Mechanisms, challenges, and therapeutic potential.Innovation (Cambridge (Mass.)) · 2026Review
- Fundamentals of Neurogastroenterology: Basic Science.Gastroenterology · 2026Review
- Betanin ameliorates dextran sulfate sodium-induced colitis in mice by modulating tight junction protein expression.Biochemistry and biophysics reports · 2026Article
- Mechanisms of chronic abdominal pain in inflammatory bowel disease and implications for treatment.Nature reviews. Gastroenterology & hepatology · 2026Review
- Hippocampal Neuronal Ferroptosis Driven by Lipocalin-2 Mediates Comorbid Visceral Pain and Anxiety in Irritable Bowel Syndrome.Molecular neurobiology · 2026Article
- GDF15 induces excessive activation of osteoclasts within the vertebral endplates leading to early endplate degeneration.JCI insight · 2026Article
- Electroacupuncture at ST36 Alleviates Visceral Hypersensitivity by Suppressing Eosinophil-Induced TRPV1 Expression on Duodenum.Pain research & management · 2026Article
- Transgenic Mouse Models to Study Enteric Glia.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Autonomic nervous system dysfunction in irritable bowel syndrome: pathophysiology and therapeutic implications.Frontiers in neuroscience · 2026Review
- Rodent Enteric Glia Culture.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Reviewing the Peripheral and Central Mechanisms of Visceral Hypersensitivity in Intestinal Disorders.International journal of medical sciences · 2026Review
- Gut Feelings Get Intense Due to Early Life Stress and Immune Imbalance.Cellular and molecular gastroenterology and hepatology · 2026Article
- Glial Connexin-43 Is a Pathogenic Mechanism Promoting Gut Inflammation in Postoperative Ileus Induced by Gut Surgical Manipulation With Potential Relevance to Humans.Cellular and molecular gastroenterology and hepatology · 2026Article
- Calcium Imaging Studies in Enteric Glia.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Implantable bioelectronics for gut electrophysiology.Nature communications · 2025Article
- Enteric glia and purinergic signaling in health and disease.Neuropharmacology · 2025Review
- Enteric glial S100B controls rhythmic colonic functions by regulating excitability and specificity in gut motor neurocircuits.The Journal of physiology · 2025Article
- The role of reactive enteric glia-macrophage interactions in acute and chronic inflammation.Neurogastroenterology and motility · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation in the intestines causes abdominal pain that is challenging to manage. The terminals of sensory neurons innervating the gut are surrounded by glia. Here, using a mouse model of acute colitis, we found that enteric glia contribute to visceral pain by secreting factors that sensitized sensory nerves innervating the gut in response to inflammation. Acute colitis induced a transient increase in the production of proinflammatory cytokines in the intestines of male and female mice. Of these, IL-1β was produced in part by glia and augmented the opening of the intercellular communication hemichannel connexin-43 in glia, which made normally innocuous stimuli painful in female mice. Chemogenetic glial activation paired with calcium imaging in nerve terminals demonstrated that glia sensitized gut-innervating nociceptors only under inflammatory conditions. This inflammatory, glial-driven visceral hypersensitivity involved an increased abundance of the enzyme COX-2 in glia, resulting in greater production and release of prostaglandin E
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.